Vaccinations Flashcards

1
Q

Briefly describe the disease caused by canine adenovirus type 1.

Contrast with the disease caused by CAV-2

A
  • CAV-1 is the cause of infectious canine hepatitis
    • CAV-2 causes respiratory disease in dogs and is genetically distinct from CAV-1
  • Adenoviruses are resistant to environmental inactivation and can survive days in fomites
    • Fomites are the likely source of natural infection
    • The virus is widespread in the wild carnivore population
  • The virus localises in the tonsils after natural infection - then regional lymph nodes, lymphatics and blood via the thoracic duct
  • The virus spreads to the liver parenchymal cells, kidney and CNS (endothelial cells) are the main targets
  • The virus is cytotoxic and can cause widespread necrosis with panlobular hepatic necrosis the major cause of death
  • Chronic hepatic damage may occur with persistence of the virus particles in the hepatic parenchyma despite and adequate antibody response (chronic latent infection)
  • Interstitial nephritis can occur due to tubular localisation of the virus
  • Corneal oedema, anterior uveitis and potentially glaucoma can occur due to viral damage of the subcorenal endothelium
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2
Q

Describe and discuss the canine adenovirus - 1 and CAV-2 vaccination and protocol

A
  • MLV CAV-2 strains are used in most vaccines
    • CAV-1 vaccines caused post-vaccine concerns including potential localisation in the kidney and nephritis
    • Inactivated vaccines were inferior and required adjuvants made them allergenic
  • Parenteral CAV-2 vaccines generate a heterotypic antibody response that is cross-protective for CAV-1
  • CAV-2 vaccine may produce mild respiratory signs if given intranasally or IV, though this is usually subclinical and mild
  • Intranasal vaccination is protective for the respiratory disease
  • Vaccination 3-4 weeks apart at 8-10 and 12-14 weeks provides long term immunity
    • 3 yearly boosters are recommended
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3
Q
A
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4
Q

Discuss the eitiology and epidemiology of canine parvovirus enteritits

A
  • CPV is a non-enveloped DNA containing virus
    • Lack of envelope ensures they are extremely stable in the environment
  • Belongs to the same subgroup as feline parvovirus
  • Many mutations have occurred with the CPV-2a, 2b and 2c strains most prevalent today
  • Maternal antibody can be protective
  • Clinical disease is often most severe when there is concurrent infection with:
    • Helminths
    • Protozoa
    • Enteric bacteria - clostridia, campylobacter, salmonella
  • Highly contagious - mostly spread by contact with contaminated faeces
  • Incubation period of 4-6 days with the newer strains
  • Disease is most severe in neonates / rapidly growing dogs < 6 months of age
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5
Q

Describe the pathogenesis of canine enteric parvovirus infection

A
  • Oronasal innoculation generally via exposure to contaminated faeces
  • Virus replication begins in the oropharyngeal lymphoid tissue and spreads to the blood via the thoracic duct
    • Eventual spread to the intestinal crypts via viraemia - this occurs 1-5 days after exposure
  • The virus destroys the germinal epithelium of the intestinal crypts
    • This leads to marked villi shortening due to impaired turnover
  • Attacks the mitotically active precursors to the leukocytes and lymphoid cells
    • Neutropenia and lymphopenia
  • Secondary bacteraemia and endotoxemia can occur due to both above mechanisms
  • Virus excretion from the intestine occurs within 3-4 days of exposure - often prior to the onset of clinical illness
  • Development of local intestinal antibody is necessary to stop intestinal shedding of the virus
  • Serum antibodies may be detected as early as 3-4 days post-infection
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6
Q

Describe the potential neurological signs with clinical canine parvovirus infection.

What are the most likely causes for the neurological signs?

A
  • CPV may directly replicate in neurological tissues
    • CPV DNA and mRNA have been identified in dogs without neurological signs
    • CPV has been identified in a range of dogs with various neurological signs, though cause and effect is not always clear
  • The changes such as cerebellar hypoplasia as seen in kittens are unlikely to be caused by CPV in dogs
  • Most neurological signs are likely to be attributable to the systemic disease caused by CPV enteritis
    • DIC / haemorrhage
    • hypoglycemia - direct neurological damage
    • endotoxemia / bacteremia
    • Sepsis
    • Acid-base / electrolyte disturbances
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7
Q

Descirbe the diagnostic tests available to assist in the diagnosis of canine parvovirus enteritis

A
  • CPV is best diagnosed by organism detection tests
    • Serological tests are less helpful as most dogs have been vaccinated
  • ELISA
    • Useful in-house at the onset of clinical disease
    • Specific but poorly sensitive
    • Virus is seldom detected past 10-12 days following natural infection
    • Intermittent shedding can reduce the sensitivity of the assay
    • Early antibody production may bind virus particles and result in false negative results
    • Can detect the various strains and weak positives may be seen following vaccination
  • Nucleic acid amplification - PCR
    • Sensitive
    • Real-time methods can give a quantitative estimate of viral DNA load
    • Peak detection at ~10 days post infection and can persistently detect virus for up to 54 days (at low levels)
    • Will detect vaccine virus in blood/faeces for up to 2 weeks
    • Can be used to identify different strains in the field and to differentiate between field and vaccine strains
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8
Q

List (and briefly describe) the major therapeutic options for treatment of severe clinical canine parvovirus infection

Note the treatments that have been studied but not found to be of benefit

A
  • IV fluids
    • Balanced electolytes especially potassium and glucose
  • Anti-microbials
    • E.coli and C. Perfringens most common secondary infections
      • Penicillin / aminoglycoside combination
      • Third generation penicillin / cephalosporin
        • Ampicillin, amoxicillin, cephtazidime, cephotaxime
      • Quinolones - not in young growing dogs
  • Anti-emetics (some controversy)
    • 5-HT3 receptor antagonists - ondansetron / dolasetron
    • metoclopramide or prochlorperazine
    • May not inhibit vomiting and may lead to hypotension
  • Early feeding / enteral feeding
    • When possible can reduce recovery time and minimise weight loss
  • Feline interferon omega
    • Survival benefit shown when started early

Not beneficial or limited evidence

  • Hyperimmune plasma - may be beneficial
  • Endotoxin anti-sera
  • Oseltamivir (Tamiflu)
  • G-CSF
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9
Q

Describe and discuss the canine parvovirus vaccination and recommended vaccination protocol

A
  • Inactivated vaccines can produce only a short lived protective response from a single injection
    • A second vaccine dise can improve the immune response which can last for ~15 months
  • MLV attenuated vaccines provide superior immunity to inactivated virus vaccines
    • Early immunity - as early as 3 days post vaccination
    • Maternal antibody can interfere
    • MLV particles can be shed in the faeces
    • The MLV disease process parallels that of wild type infection
    • A single vaccine produces long-lived immunity as shown by rechallenge data
      • 3-7 years
  • Vaccination is recommended at 6-8 weeks, then each 2-4 weeks until 16 weeks of age
    • The variation depends on the relative risk of exposure and potential viral load
    • Early finish vaccines (10 weeks) may not be protective 100% of the time due to persistence of maternal antibody
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10
Q

Describe and discuss the canine distemper virus vaccination and recommended vaccination protocol

A
  • Maternal antibody is transferred in colostrum and has a half life of 8.4 days
    • MDA are usually absent by 12-14 weeks
  • Vaccines are given at 6-8 weeks and then each 3-4 weeks until 16 weeks of age
  • Adequate immunity requires two doses of vaccine, despite the absence of maternal antibodies, 2-4 weeks apart
  • Vaccination may provide protective antibodies for 3-7 years, however antibody titres alone are not predictive of immunity to clinical disease
  • The most highly protective MLV are more likely to cause clinical illness, whereas they are also most likely to induce “sterilising immunity”
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11
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12
Q

Describe and discuss the feline parvovirus vaccination and recommended vaccination protocol

A
  • Maternal antibodies have a half life of ~9.5 days
  • Successful vaccination requires a reduction in MDA which occurs from 6.8-18 weeks depending on the antibody titre in the queen and the transfer of colostrum
    • Therefore in kittens from queens in endemic areas should have their final vaccination no earlier than 16 weeks of age
  • Inactivated vaccines need a booster to provide adequate protection
    • CMI has been demonstrated as early as 3-7 days post second vaccine
    • Immunity can last for 7.5 years - long term
  • MLV vaccine will produce a neutralising titre of 8-10 after a single vaccine - likely protective long term
    • Booster is still recommended
  • The vaccination program varies from client owned to shelter cats
    • Shelter cats should be vaccinated earlier (from 4 weeks) and each 2-3 weeks thereafter while at risk of exposure until ~14-16 weeks.
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13
Q
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